Project description:Idiopathic pulmonary fibrosis is a devastating aging-associated disease of unknown etiology. Despite that aging is a major risk factor, the mechanisms linking aging with this disease are uncertain, and experimental models to explore them in lung fibrosis are scanty. We examined the fibrotic response to bleomycin-induced lung injury in Zmpste24-deficient mice, which exhibit nuclear lamina defects developing accelerated aging. We found that young WT and Zmpste24(-/-) mice developed a similar fibrotic response to bleomycin. Unexpectedly, while old WT mice developed severe lung fibrosis, accelerated aged Zmpste24-/- mice were protected showing scant lung damage. To investigate possible mechanisms associated with this resistance to fibrosis, we compared the transcriptome signature of the lungs and found that Zmpste24(-/-) mice showed downregulation of several core and associated matrisome genes compared with WT mice. Interestingly, some microRNAs that target extracellular matrix molecules such as miR23a, miR27a, miR29a, miR29b-1,miR145a, and miR491 were dysregulated resulting in downregulation of profibrotic pathways such as TGF-β/SMAD3/NF-κB and Wnt3a/β-catenin signaling axis. These results indicate that the absence of Zmpste24 in aging mice results in impaired lung fibrotic response after injury, which is likely associated to the dysregulation of fibrosis-related miRNAs. Aging is a driving force of pulmonary fibrosis. Mice laking Zmpste24 have an accelerated aging phenotype. During the development of the disease there are several extracellular matrix genes, principally collagens upregulated. We use microarray to unveil changes associated with the pulmonary response in aged mice
Project description:This SuperSeries is composed of the following subset Series: GSE36420: Gene expression profiling of C57BL/6 mouse lung tissue with various treatments using the MA07 array GSE36421: Gene expression profiling of C57BL/6 mouse lung tissue with various treatments using the MA10 array GSE36422: Gene expression profiling of C57BL/6 mouse lung tissue with various treatments using the MA11 array Refer to individual Series
Project description:Our study looks at the dirsruption of lung circadian transcriptome that occurs when neutrophils are depleted (by application of antibodies (anti-Ly6G-1A8) to wildtype C57BL/6 mice, or Diphtheria toxin (DT) to neutrophil-specific DT-susceptible mice (MRP8-Cre;iDTR-flox)).
Project description:Cy3-labeled cDNA obtained from four pools of three hearts of neonatal C57BL Cx43 null mice were compared to Cy3-labeled cDNA obtained from four pools of three hearts of neonatal C57BL wildtype mice through Cy5-labeled sample reference prepared at once for the entire experiment from aorta, brain, heart, kidney, liver, lung, ovary/testicles, spleen, and stomach - equal amounts from adult male and female C57BL mice. Keywords = Cx32 null vs wildtype neonatal mouse heart Keywords: parallel sample
Project description:To investigate the aging-associated gene expression in lung tissue of the National Center for Geriatrics and Gerontology (NCGG) Aging Farm mice, RNA was prepared from lung of the male 3-, 6-, 12- and 24-month-old C57Bl/6J mice. RNA was subjected to RNA-seq and the gene expression profiling analysis.